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Vascular leakage and hemorrhagic syndrome are the clinical features associated with dengue infection, yet the mechanisms remain unclear. In this study, the cross\u2010reactivity of dengue patient sera with endothelial cells was demonstrated. There were higher percentages of endothelial cells reactive with dengue hemorrhagic fever\/dengue shock syndrome patient sera than those with dengue fever patient sera. The percentages of endothelial cells reactive with patient serum IgM were higher than those with IgG. Further studies showed that the endothelial cell binding activity was inhibited by pretreatment with dengue virus nonstructural protein 1 (NS1). The antibodies against NS1 produced after dengue virus infection may, at least in part, account for the cross\u2010reactivity of patient sera with endothelial cells. Furthermore, dengue patient sera induced endothelial cell apoptosis via a caspase\u2010dependent pathway that was also inhibited by NS1 pretreatment. In addition to apoptosis, patient sera caused cell lysis in the presence of complement, and DHF\/DSS patient sera showed higher percentages of cytotoxicity than dengue fever patient sera. Thus, the generation of cross\u2010reactive autoantibodies against endothelial cells would lead to their dysfunction, which may play a role in the pathogenesis of dengue virus infection. J. Med. Virol. 69:82\u201390, 2003. \u00a9 2003 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jmv.10261","type":"journal-article","created":{"date-parts":[[2002,11,18]],"date-time":"2002-11-18T13:44:13Z","timestamp":1037627053000},"page":"82-90","source":"Crossref","is-referenced-by-count":172,"title":["Antibodies from dengue patient sera cross\u2010react with endothelial cells and induce 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